Acute Guillain-Barr[unreadable] syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) are acquired human demyelinating diseases of the unknown etiology and pathogenesis. Much evidence points to immunological mechanisms of tissue injury in these diseases often following an infectious trigger in GBS. The established therapeutic efficacy of plasmapheresis in GBS and CIDP suggests that autoantibodies or circulating immune factors are paramount in the pathogenesis of these disorders. Recent evidence indicates that major acidic glycolipids such as GM1, LM1, GD1a and GT1b are important antigens in about half of the patients with GBS. However, the antigenic specificity in most of the other GBS patients remains unknown. We have found that a proportion of patients with GBS react with GT1b, a minor ganglioside. We hypothesize that the antigens in the GBS patients not reactive with major gangliosides, are minor as yet not well characterized glycolipids or proteins/glycoproteins. The specific aim of this study is identify and characterize glycolipid and protein antigens in GBS patients that do not exhibit autoantibodies against major ganglioside antigens. We propose to test sera from a large number of patients with GBS, CIDP and controls, for autoantibodies to proteins and minor glycolipid antigens, and to purify and characterize the putative protein or glycolipid antigen(s). PAGE-Western blotting, enzyme linked immunosorbent assay (ELISA) and thin-layer chromatogram-immunostaining will be used to test for antineural antibodies. Early and serial serum specimens from GBS and CIDP patients will be examined to see whether autoantibody titers correlate with disease severity.